Mycoplasma hyorhinis is an etiologic agent causing degenerative polyarthritis in its natural host, the swine. This disease displays characteristic features of other mycoplasmoses, including chronicity and associated immunopathological phenomena. Both of these characteristics may ultimately arise from the propensity of mycoplasmas to colonize surfaces of host cells, possibly resulting in the simultaneous stimulation of destructive immunological reactions, and evasion of host-immune responses. Surface membrane constituents of mycoplasmas are centrally important as potential mediators of mycoplasma-host cell interactions, and as targets of this response. It is proposed to investigate molecular aspects and immunological consequences of mycoplasma-cell interactions using an in vitro model of murine T-lymphoblastoid cells chronically infected with M. hyorhinis. An established set of defined monoclonal antibodies to M. hyorhinis surface antigens will be utilized: 1) to investigate mechanistic features of an antibody-mediated cytopathogenic effect selectively occurring in cultures of mycoplasma-colonized cells, 2) to identify surface structures potentially involved in mycoplasmal attachment and transfer during chronic infections, 3) to define corresponding mycoplasma epitopic surface structures recognized by host antibodies during arthritic disease in swine, and 4) to immunochemically characterize molecules bearing these selected surface epitopes. A separate monoclonal antibody raised against M. hyorhinis and shown to react with mammalian intermediate filaments will be utilized to characterize a protein antigen, demonstrated in numerous mycoplasma species, representing a specific case of antigenic mimicry possibly responsible for "autoimmune" reactions associated with mycoplasmal infections. Immunocytochemical, micrographic, and immunbiochemical techniques will be utilized throughout this project. It is anticipated that the structural and functional dissection of specific molecules mediating mycoplasma-host cell interactions will contribute to the understanding of immunopathogenic phenomena in chronic mycoplasma diseases.